Ransberry Victoria E, Morash Andrea J, Blewett Tamzin A, Wood Chris M, McClelland Grant B
Department of Biology, McMaster University, Hamilton, ON L8S 4K1, Canada.
CSIRO Marine and Atmospheric Research, GPO Box 1538, Hobart, TAS 7001, Australia.
Aquat Toxicol. 2015 Apr;161:242-52. doi: 10.1016/j.aquatox.2015.02.013. Epub 2015 Feb 21.
In freshwater (FW), many of the main mechanisms of copper (Cu) toxicity have been characterized; however, toxicity mechanisms in seawater (SW) are less well understood. We investigated the effects of salinity on Cu-induced oxidative stress and metabolic responses in adult killifish, Fundulus heteroclitus. We exposed FW and SW-acclimated killifish to either low Cu (LC, 50 μg/L) or high Cu (HC, 200 μg/L) for 96 h and compared them to controls (CTRL) under the same salinities without added Cu. Cu exerted minimal influence on tissue ion levels in either FW or SW. Salinity generally protected against Cu bioaccumulation in the gills and liver, but not in the carcass. Hematocrit (Hct) and hemoglobin (Hb) levels were increased by LC and HC in both FW and SW, and blood lactate was reduced in FW-killifish exposed to LC and HC. Rates of oxygen consumption were similar across treatments. Salinity reduced Cu load in gill, liver and intestine at LC but only in the gills at HC. In general, Cu increased gill, liver, and intestine catalase (CAT) activity, while superoxide dismutase (SOD) either decreased or remained unchanged depending on tissue-type. These changes did not directly correlate with levels of protein carbonyls, used as an index of oxidative stress. Cu-induced changes in carbohydrate metabolic enzymes were low across tissues and the effect of salinity was variable. Thus, while salinity clearly protects against Cu bioaccumulation in some tissues, it is unclear whether salinity protects against Cu-induced oxidative stress and metabolic responses.
在淡水（FW）环境中，铜（Cu）毒性的许多主要机制已得到明确；然而，海水（SW）环境中的毒性机制却了解得较少。我们研究了盐度对成年鳉鱼（Fundulus heteroclitus）铜诱导的氧化应激和代谢反应的影响。我们将适应淡水和海水环境的鳉鱼暴露于低铜（LC，50μg/L）或高铜（HC，200μg/L）环境中96小时，并将它们与相同盐度下未添加铜的对照组（CTRL）进行比较。铜对淡水或海水中的组织离子水平影响极小。盐度通常能防止鳃和肝脏中铜的生物积累，但对鱼体躯并无此作用。在淡水和海水中，低铜和高铜处理均使血细胞比容（Hct）和血红蛋白（Hb）水平升高，而暴露于低铜和高铜环境的淡水鳉鱼血液乳酸水平降低。各处理组的耗氧率相似。在低铜处理时，盐度降低了鳃、肝脏和肠道中的铜含量，但在高铜处理时仅降低了鳃中的铜含量。总体而言，铜增加了鳃、肝脏和肠道中的过氧化氢酶（CAT）活性，而超氧化物歧化酶（SOD）则根据组织类型降低或保持不变。这些变化与用作氧化应激指标的蛋白质羰基水平并无直接关联。铜诱导的碳水化合物代谢酶变化在各组织中较低，且盐度的影响各不相同。因此，虽然盐度显然能防止某些组织中铜的生物积累，但盐度是否能防止铜诱导的氧化应激和代谢反应尚不清楚。
